Ergot is a fungal disease of small grains and grasses. It reduces yield and quality of grain, and causes ergotism when consumed by humans or livestock. The fungus Claviceps purpurea infects seed heads at flowering and replaces the grain with fungal sclerotia. It is these sclerotia that cause ergotism when consumed. While extremely rare today, ergotism in humans was common in the Middle Ages due to contaminated rye bread.

Fortunately, ergot is very easy to see in standing or harvested grain and grasses.

Ergot sclerotia in malting barley

Ergot has an interesting disease cycle. Sclerotia develop during the spring and summer in grains and grasses (1). The sclerotia then fall to the ground and overwinter on the surface of the soil (2). The following spring, the sclerotia germinate and shoot spores into the air (3). These spores land on the open flowers of grains or grasses and invade the embryo of the developing seed. A sweet "honey-dew" is produced that attracts insects who then spread spores to other plants (4), continuing the cycle.

Image credit: North Dakota State University Extension

Control of Ergot in Small Grains

There are no chemicals labeled for control of ergot so we must rely on cultural practices to reduce ergot in the fields and surrounding environment. Use ergot-free seed and rotate fields out of cereal production for at least 1 year. Grasses are an important host for ergot, and a source of secondary infection. Mowing and grazing grasses along field edges, ditch banks, and fence rows will reduce the amount of ergot that can cause infection.

Ergot sclerotia rarely survive for more than a year on the soil. While the sclerotia may survive in the soil for up to two years, they will not germinate if buried to a depth of at least 1 inch (source).

High temperatures destroy ergot sclerotia. While surface temperatures vary under field burning, the grass seed industry has had success using burning to reduce, but not eliminate ergot. Research has shown that destruction of 100% of the sclerotia requires 116 seconds at 200F , 48 seconds at 300F, and 15 seconds at 400F.

There is some evidence that low soil micronutrient levels (especially copper) increases the likelihood of ergot infection. Copper deficiency can cause prolonged flowering in small grains, which increased the window for ergot infection.

Weather greatly influences ergot infection. Wet weather and soil favors the germination of ergot on the soil in the spring. Cool, wet weather during flowing favors the initial infection and development of the initial floret and "honey-dew".

Livestock or poultry that consume even small amounts of contaminated grains or grasses can develop clinical symptoms of ergotism. Cattle are more susceptible than sheep. Symptoms can vary based on several factors, but often include the following:

Excitability, staggering, convulsions, backward arching of the back

Gangrenous tissue on feet and sloughing of tissue on ears and tails

Low milk production, rough coat, weight loss

The only cure for ergotsm is to identify and remove the contaminated feed source.